Compositions and methods are provided for treating fibrosis in a mammal by administering a therapeutic dose of a pharmaceutical composition.
Legal claims defining the scope of protection. Each claim is shown in both the original legal language and a plain English translation.
1. A method for in vivo reversion of fibrosis of the lungs in a mammalian patient, the method comprising: administering an antibody that neutralizes CD47 to the mammalian patient in a dose effective to reverse fibrosis in vivo.
This invention relates to a method for treating lung fibrosis in mammals by administering an antibody that neutralizes CD47. Fibrosis is a condition characterized by excessive scarring and stiffening of lung tissue, leading to impaired respiratory function. The method involves delivering an anti-CD47 antibody in a dosage sufficient to reverse fibrosis within the patient's body. CD47 is a protein that inhibits phagocytosis, a process where immune cells remove damaged or dead cells. By blocking CD47, the antibody promotes the clearance of fibrotic tissue, allowing the lungs to regain normal function. The treatment leverages the body's natural immune response to degrade scar tissue, offering a targeted approach to fibrosis reversal. The method is applicable to any mammalian patient suffering from lung fibrosis, providing a therapeutic option where conventional treatments may be limited. The key innovation lies in using CD47 neutralization to trigger immune-mediated clearance of fibrotic deposits, addressing the underlying pathology rather than just symptoms. This approach may offer a more effective and durable solution for patients with progressive lung fibrosis.
2. The method of claim 1 , wherein the antibody is co-administered with an anti-VEGF agent.
This invention relates to a method for treating a disease or condition in a subject by administering an antibody that binds to a specific target, combined with an anti-VEGF (vascular endothelial growth factor) agent. The antibody is designed to inhibit or modulate a biological pathway involved in the disease, while the anti-VEGF agent works to reduce angiogenesis or vascular permeability, which are often associated with disease progression. The co-administration of these two agents enhances therapeutic efficacy by targeting multiple disease mechanisms simultaneously. The antibody may be a monoclonal antibody, polyclonal antibody, or antibody fragment, and it is administered in a therapeutically effective amount. The anti-VEGF agent may include bevacizumab, ranibizumab, or other VEGF inhibitors. The method is particularly useful for treating conditions such as cancer, macular degeneration, or inflammatory diseases where both immune modulation and angiogenesis inhibition are beneficial. The combination therapy may reduce side effects or improve patient outcomes compared to monotherapy. The invention also includes variations in dosing, administration routes, and treatment schedules to optimize therapeutic effects.
3. The method of claim 1 , wherein pathogenic fibroblasts of the fibrosis have elevated levels of c-Jun.
This invention relates to a method for treating fibrosis by targeting pathogenic fibroblasts that exhibit elevated levels of the c-Jun protein. Fibrosis is a condition characterized by excessive deposition of extracellular matrix components, leading to tissue scarring and organ dysfunction. The method involves identifying and selectively inhibiting these pathogenic fibroblasts, which are implicated in the progression of fibrosis due to their abnormal activity and elevated c-Jun expression. The approach may include therapeutic interventions such as administering agents that reduce c-Jun activity or targeting pathways regulated by c-Jun to mitigate fibrosis. The method may also involve diagnostic steps to detect elevated c-Jun levels in fibroblasts, ensuring precise identification of pathogenic cells. By focusing on these specific fibroblasts, the treatment aims to disrupt the fibrotic process while sparing healthy tissue, offering a more targeted and effective approach to fibrosis management. The invention addresses the need for therapies that specifically address the underlying cellular mechanisms driving fibrosis, rather than broadly suppressing fibroblast activity, which can have unintended side effects.
4. The method of claim 1 , wherein the patient has been diagnosed by the method comprising: determining the presence of elevated levels of CD47 in a patient biological sample.
This invention relates to a diagnostic method for identifying patients with elevated CD47 levels, which is associated with certain medical conditions. The method involves analyzing a biological sample from a patient to detect and quantify CD47, a protein that plays a role in immune regulation and cell survival. Elevated CD47 levels may indicate the presence of diseases such as cancer, autoimmune disorders, or other conditions where abnormal cell proliferation or immune evasion occurs. The diagnostic process includes obtaining a biological sample, such as blood, tissue, or bodily fluids, and using analytical techniques like flow cytometry, immunohistochemistry, or molecular assays to measure CD47 expression. The method may also involve comparing the detected CD47 levels against a reference threshold to determine if they are abnormally high. This diagnostic approach helps in early disease detection, treatment planning, and monitoring of therapeutic responses. The invention may be used in conjunction with other diagnostic tools to provide a comprehensive assessment of a patient's condition.
5. The method of claim 1 , wherein the patient has been diagnosed by the method comprising: determining the presence of elevated levels of c-Jun in a patient biological sample.
This invention relates to a method for diagnosing a medical condition by detecting elevated levels of the c-Jun protein in a patient's biological sample. The method involves analyzing a biological sample, such as blood, tissue, or other bodily fluids, to measure the concentration of c-Jun. Elevated levels of c-Jun are indicative of a specific medical condition, allowing for early detection and diagnosis. The method may include steps such as sample preparation, protein extraction, and quantitative analysis using techniques like immunohistochemistry, Western blotting, or enzyme-linked immunosorbent assays (ELISA). The detection of c-Jun serves as a biomarker for the condition, enabling clinicians to assess disease progression or treatment response. The method may be used in conjunction with other diagnostic tools to improve accuracy. The invention addresses the need for reliable, non-invasive, or minimally invasive diagnostic techniques to identify conditions associated with c-Jun overexpression, facilitating timely medical intervention.
6. The method of claim 1 , wherein the patient has been analyzed after prevention or treatment by a method comprising: determining the extent of fibrosis in a patient biological sample.
This invention relates to medical diagnostics, specifically methods for assessing fibrosis in patients following prevention or treatment. Fibrosis is the thickening and scarring of connective tissue, often resulting from chronic inflammation or injury, and accurate assessment is critical for monitoring disease progression and treatment efficacy. The method involves analyzing a biological sample from a patient to determine the extent of fibrosis. The analysis may include histological examination, biochemical assays, or imaging techniques to quantify fibrotic tissue. The method is particularly useful for evaluating the effectiveness of anti-fibrotic therapies or preventive measures. By measuring fibrosis levels, clinicians can make informed decisions about treatment adjustments or further interventions. The invention addresses the need for reliable, objective fibrosis assessment to improve patient outcomes in conditions such as liver cirrhosis, pulmonary fibrosis, and cardiovascular disease. The method may be integrated into routine clinical practice to provide real-time feedback on treatment progress.
7. A method for in vivo reversion of fibrosis of the lungs in a mammalian patient, the method comprising: administering an antibody that neutralizes CD47 to the mammalian patient in combination with an anti-VEGF agent, in a dose effective to reverse fibrosis in vivo.
This invention relates to a method for treating lung fibrosis in mammals by combining an antibody that neutralizes CD47 with an anti-VEGF agent. Fibrosis is a condition characterized by excessive tissue scarring, leading to impaired lung function. The method involves administering these agents in doses sufficient to reverse fibrosis in living tissue. The CD47-neutralizing antibody disrupts signaling pathways that contribute to fibrosis progression, while the anti-VEGF agent inhibits vascular endothelial growth factor, which plays a role in fibrosis development. The combination of these treatments enhances the reversal of fibrotic tissue, restoring normal lung function. The approach targets both immune and vascular mechanisms involved in fibrosis, providing a more comprehensive therapeutic effect than single-agent treatments. This method is particularly useful for patients with advanced fibrosis who have not responded to conventional therapies. The invention leverages the synergistic effects of CD47 neutralization and VEGF inhibition to achieve significant fibrosis regression in vivo.
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February 28, 2018
March 29, 2022
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